Hydrogen Gas Inhalation Attenuates Seawater Instillation-Induced Acute Lung Injury via the Nrf2 Pathway in Rabbits

Diao, Mengyuan; Zhang, Sheng; Wu, Li-Feng; Huan, Le; Huang, Fenglou; Cui, Yunliang; Zhou, Lin

doi:10.1007/s10753-016-0440-1

Cited by 40 publications

(26 citation statements)

References 27 publications

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“…How HRS activates the HIF-1 α pathway to induce autophagy remains unclear. There are two ways of enhancing the activity of HIF-1 α , either to enhance the synthesis of HIF-1 α , such as gene transfer or to inhibit the degradation of HIF-1 α [ 51 ]. Subsequent studies have indicated that the anti-inflammatory effect of hydrogen may activate Nrf2 [ 51 ] and its downstream target, heme oxygenase-1 (HO-1), in different experimental models [ 52 ].…”

Section: Discussionmentioning

confidence: 99%

“…There are two ways of enhancing the activity of HIF-1 α , either to enhance the synthesis of HIF-1 α , such as gene transfer or to inhibit the degradation of HIF-1 α [ 51 ]. Subsequent studies have indicated that the anti-inflammatory effect of hydrogen may activate Nrf2 [ 51 ] and its downstream target, heme oxygenase-1 (HO-1), in different experimental models [ 52 ]. Previous studies have indicated that HO-1 can trigger and regulate HIF-1 α expression in hypoxic tumor cells [ 53 ].…”

Section: Discussionmentioning

confidence: 99%

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Hydrogen-Rich Saline Activated Autophagy via HIF-1α Pathways in Neuropathic Pain Model

Wang

Huo

Chen

et al. 2018

BioMed Research International

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Background Neuropathic pain is a chronic and intractable pain, with very few effective analgesics. It involves an impaired cell autophagy process. Hydrogen-rich saline (HRS) reportedly reduces allodynia and hyperalgesia in a neuropathic pain model; however, it is unknown whether these effects involve autophagy induction. Methods We investigated the relationship between HRS and cell autophagy in a neuropathic pain model generated by chronic constriction injury (CCI) in Sprague–Dawley rats. Rats received an intraperitoneal injection of HRS (10 mL/kg daily, from 1 day before until 14 days after CCI), 3MA (autophagy inhibitor), 2ME2 (HIF-1α inhibitor), or EDHB (HIF-1α agonist). The mechanical withdrawal threshold (MWT) and thermal withdrawal latency (TWL) were tested 1 day before and 1, 3, 7, 10, and 14 days after the operation. HIF-1α and cell autophagy markers in the spinal cord were evaluated by western blotting and real-time PCR assays at 14 days after CCI. Autophagosomes with double membranes were identified by transmission electron microscopy. Results CCI caused behavioral hypersensitivity to mechanical and thermal stimulation in the hind-paw of the injured side. HRS improved MWT and TWL, activated autophagy, and increased autophagosomes and autolysosomes in CCI rats. 3-MA aggravated hyperalgesia and allodynia and suppressed autophagy, while EDHB attenuated hyperalgesia and activated the autophagy procedure and the HIF-1α downstream target gene BNIP3. HIF-1α inhibitors reversed the regulatory effects of HRS on autophagy in CCI rats at 14 days after spinal cord injury. Conclusion HRS reduced mechanical hyperalgesia and activation of cell autophagy in neuropathic pain through a HIF1-dependent pathway.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Hydrogen-Rich Saline Activated Autophagy via HIF-1α Pathways in Neuropathic Pain Model

Wang

Huo

Chen

et al. 2018

BioMed Research International

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“…Since the first report in 2007, (5) accumulating evidence has demonstrated its therapeutic potential against IRI and the underlying mechanisms therein. Currently, H 2 i s known to have 3 definitive effects: antioxidant, (5)(6)(7)(8)(9)(10)(11)(12)(13) anti-inflammatory, (10,(14)(15)(16) and antiapoptosis. (8,17) Though some experimental animal studies have shown its therapeutic potential in organ preservation, eg, lung, (11) heart, (18) kidney, (6) intestine, (7) and liver, (19,20) its clinical use is yet to be applied because of its unfavorable features.…”

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confidence: 99%

Hydrogen Flush After Cold Storage as a New End‐Ischemic Ex Vivo Treatment for Liver Grafts Against Ischemia/Reperfusion Injury

Tamaki¹,

Hata²,

Okamura³

et al. 2018

Liver Transpl

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Cold storage (CS) remains the gold standard for organ preservation worldwide, although it is inevitably associated with ischemia/reperfusion injury (IRI). Molecular hydrogen (H ) is well known to have antioxidative properties. However, its unfavorable features, ie, inflammability, low solubility, and high tissue/substance permeability, have hampered its clinical application. To overcome such obstacles, we developed a novel reconditioning method for donor organs named hydrogen flush after cold storage (HyFACS), which is just an end-ischemic H flush directly to donor organs ex vivo, and, herein, we report its therapeutic impact against hepatic IRI. Whole liver grafts were retrieved from Wistar rats. After 24-hour CS in UW solution, livers were cold-flushed with H solution (1.0 ppm) via the portal vein (PV), the hepatic artery (HA), or both (PV + HA). Functional integrity and morphological damages were then evaluated by 2-hour oxygenated reperfusion at 37°C. HyFACS significantly lowered portal venous pressure, transaminase, and high mobility group box protein 1 release compared with vehicle-treated controls (P < 0.01). Hyaluronic acid clearance was significantly higher in the HyFACS-PV and -PV + HA groups when compared with the others (P < 0.01), demonstrating the efficacy of the PV route to maintain the sinusoidal endothelia. In contrast, bile production and lactate dehydrogenase leakage therein were both significantly improved in HyFACS-HA and -PV + HA (P < 0.01), representing the superiority of the arterial route to attenuate biliary damage. Electron microscopy consistently revealed that sinusoidal ultrastructures were well maintained by portal HyFACS, while microvilli in bile canaliculi were well preserved by arterial flush. As an underlying mechanism, HyFACS significantly lowered oxidative damages, thus improving the glutathione/glutathione disulfide ratio in liver tissue. In conclusion, HyFACS significantly protected liver grafts from IRI by ameliorating oxidative damage upon reperfusion in the characteristic manner with its route of administration. Given its safety, simplicity, and cost-effectiveness, end-ischemic HyFACS may be a novel pretransplant conditioning for cold-stored donor organs.

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“…Treatment with AL decreased MPO activity in lung tissue. Cellular lipid peroxidation results in MDA generation, which causes cross‐linking and polymerization of proteins and nucleic acids, exerting cytotoxic effects . In this study, AL treatment decreased the MDA content.…”

Section: Discussionmentioning

confidence: 50%

Alkannin attenuates lipopolysaccharide‐induced lung injury in mice via Rho/ROCK/NF‐κB pathway

Lin

Hou

et al. 2019

J Biochem & Molecular Tox

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We investigated the effects and associated mechanism of alkannin (AL) on lipopolysaccharide (LPS)-induced acute lung injury in a mouse model. Pretreatment with AL in vivo significantly reduced the lung wet/dry weight ratio and inhibited lung myeloperoxidase activity and malondialdehyde content, while increasing superoxide dismutase activity. Hematoxylin and eosin staining demonstrated that AL attenuated lung histopathological changes. In addition, AL-inhibited overproduction of proinflammatory cytokines in bronchoalveolar lavage fluid and lung tissues in LPS-injured mice and LPS-exposed A549 cells. Further analysis showed that AL-inhibited induction of the Rho/ROCK/NF-κB pathway via LPS-induced inflammation in mice and A549 cells. Fasudil, a selective ROCK inhibitor, showed similar effects. Overall, the findings indicate that AL suppresses the expression of messenger RNAs and proteins associated with Rho/ROCK/NF-κB signaling to effectively ameliorate lung injury. K E Y W O R D S alkannin, lipopolysaccharide, lung injury, Rho/ROCK/NF-κB

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Hydrogen Gas Inhalation Attenuates Seawater Instillation-Induced Acute Lung Injury via the Nrf2 Pathway in Rabbits

Cited by 40 publications

References 27 publications

Hydrogen-Rich Saline Activated Autophagy via HIF-1α Pathways in Neuropathic Pain Model

Hydrogen-Rich Saline Activated Autophagy via HIF-1α Pathways in Neuropathic Pain Model

Hydrogen Flush After Cold Storage as a New End‐Ischemic Ex Vivo Treatment for Liver Grafts Against Ischemia/Reperfusion Injury

Alkannin attenuates lipopolysaccharide‐induced lung injury in mice via Rho/ROCK/NF‐κB pathway

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